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. 2020 Jun 22;12(6):671.
doi: 10.3390/v12060671.

Flavivirus Infection Associated with Cerebrovascular Events

Cássia F Estofolete  1 , Bruno H G A Milhim  1 , Nathalia Zini  1 , Samuel N Scamardi  1 , Joana D'Arc Selvante  1 , Nikos Vasilakis  2   3   4   5 , Maurício L Nogueira  1
Affiliations

Flavivirus Infection Associated with Cerebrovascular Events

Cássia F Estofolete et al. Viruses. .

Abstract

Arthropod-borne viruses (arboviruses) of the genus Flavivirus are distributed globally and cause significant human disease and mortality annually. Flavivirus infections present a spectrum of clinical manifestations, ranging from asymptomatic to severe manifestations, including hemorrhage, encephalitis and death. Herein, we describe 3 case reports of cerebrovascular involvement in patients infected by dengue and Zika viruses in Sao Jose do Rio Preto, São Paulo State, Brazil, a hyperendemic area for arbovirus circulation, including dengue, yellow fever, chikungunya and Saint Louis encephalitis viruses. Our findings highlight the potential threat that unusual clinical manifestations may pose to arbovirus disease management and recovery.

Keywords: Zika virus; atypical manifestations; cerebrovascular events; dengue virus.

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Conflict of interest statement

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses or interpretation of data; in the writing of the manuscript or in the decision to publish the results.

Figures

Figure 1
Figure 1
Brain radiologic imaging of patient 1. (A) No evidence of mass or vascular lesions in cerebellum or (B) occipital lobes (OL) in brain computed tomography (CT) immediately after seizure and decerebrate posturing events (10 days post onset of dengue symptoms). (C) T1 weighted image from brain nuclear magnetic resonance (NMR) performed 24 h after occurrence of disorientation and seizures, with evidence of ischemia in cerebellum (C) (11 days post onset of dengue symptoms). (D) Ischemic areas in thalamus (T) and occipital lobe. (E,F) Extensive ischemic infarct in cerebellum and parietal lobe (PL), in diffusion-weighted and fluid-attenuated inversion recovery (FLAIR) image from brain NMR performed 24 h after occurrence of acute clinical events (disorientation and seizures), respectively. (G) Ischemic infarct in thalamus and occipital lobe. (H) No evidence of vessel lesions, including basilar and vertebral arteries responsible to vascularization of injured areas in brain angiographic study performed 24 h after seizures.
Figure 2
Figure 2
Patient 2 radiologic observations. (A) Brain no-contrast computed tomography with hypodense images in right parieto-occipital (0.5 cm—arrowhead) and left front-temporal (1.6 cm—red star) areas. (B) Corresponding brain contrasted computed tomography with middle-line deviation (red line) compared to regular condition (yellow line). It is not possible to view left lateral ventricular and cerebellar cisterns due to compression by left subarachnoid hemorrhage.
Figure 3
Figure 3
Patient 3 radiologic observations. Brain NMR performed 48 h after admission. Red arrowhead shows ischemic infarct in cerebellum (A), cerebellum (B), base nuclei (C) and hippocampus (D) in FLAIR (A) and diffusion-weighted image (B–D). (E,F) Stenosis in medium cerebral artery and stenosis in basilar artery, respectively.
See this image and copyright information in PMC

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